Increased activation of autoreactive B cells in iNKT cell–deficient mice. (A) WT and NKT-deficient mice (Jα18^−/− and CD1d^−/−) injected four times i.v. with syngenic apoptotic cells. Serum IgG anti-DNA response is followed preimmune (PI) to day 61. (B) IgG3 anti-DNA PI and day 33. (C) IgG reactivity against lipid antigens (cardiolipin and PC) PI and day 33. (D) Representative kidney histology from day 61. 10× and 100× magnification of IgG immune complex (IC) deposition, H&E staining, and quantification of IC deposition (score 0–3). Bars: 300 µm (low); 47 µm (high). (E) FACS plot showing MZB cell gating of viable CD19⁺ splenocytes and quantification of the MZB cells in WT and NKT^−/− mice. (F) IgG response to the T cell–independent type II antigen TNP-Ficoll in WT and NKT^−/− mice. (G) IgG response to the T cell–dependent antigen NP-OVA in WT and CD1d^−/−. (H) IgM anti-PC in serum of untreated WT and CD1d^−/− mice. (I) IgG anti-DNA response after ex vivo stimulation of splenocytes with LPS for 72 h. Antibody levels (A–C and F–I) were measured by ELISA. Results expressed as mean ± SEM in A–C (n = 6–8), E (n = 5), F (n = 10–11), G (n = 6), I (n = 3), and individual mice and mean in D (n = 7–8) and H (n = 35–42). n.s., not significant. *, P < 0.05; **, P < 0.01. In A, the significance is related to the WT response. Data are representative of at least two independent experiments or (H) pooled from three independent experiments.